Hearts have ability to sense mechanical stimuli and transform into adaptive changes in cardiac function by a process called mechanotransduction. Under prolonged overload this process becomes maladaptive, leading to the development of cardiac diseases such as ventricular hypertrophy and ultimately to heart failure.
The Cardiac Mechanotransduction research group in the Cardiovascular Research Center includes both basic and translational investigations of mechanotransduction aimed at developing novel therapeutic approaches to mitigate heart failure remodeling. In the mechanotransduction laboratory, researchers target modulating intercalated disc, a specialized type of cell-cell contact, which is a center of mechanotransduction that promote cardiomyocyte de-differentiation and proliferation. Using various transgenic animal models, cardiac mechanotransduction research program investigates the relationship between cardiac mechanics, function, and growth in the normal and diseased heart.
The Cardiac Mechanotransduction research program is an integrative program with the Heart Rhythm Disorder research program in the Cardiovascular Research Center. Special interests include mechanotransduction in triggering cardiac arrhythmias such as atrial fibrillation and arrhythmogenic right ventricular cardiomyopathy. Combined with basic research and samples from patients, the Cardiac Mechanotransduction research group aims at finding innovative treatments through modulating intercalated disc to prevent cardiac arrhythmias.
“Cardiomyocyte orientation modulated by the Numb family proteins-N-cadherin axis is essential for ventricular wall morphogenesis “ (https://pubmed.ncbi.nlm.nih.gov/31300538/)
“Alpha-catenins control cardiomyocyte proliferation by regulating Yap activity” (https://pubmed.ncbi.nlm.nih.gov/25305307/)
“Niche Cadherins Control the Quiescence-to-Activation Transition in Muscle Stem Cells” (https://pubmed.ncbi.nlm.nih.gov/29166613/)